HIV-1 Regulatory Protein Expression in Tissues of Infected and Uninfected Individuals

2015 ◽  
pp. 130-139
Author(s):  
Henk K. Parmentier ◽  
Henk-Jan Schuurman ◽  
Dick F. van Wichen ◽  
Frits H. J. Gmelig Meyling ◽  
Jaap Goudsmit
Keyword(s):  
Protein Expression ◽  
Regulatory Protein ◽  
Hiv 1

2040-P: Chronic Activation of CREB by Islet Amyloid Increases Star (Steroidogenic Acute Regulatory Protein) Expression in Islets

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2040-P
Author(s):  
MEGHAN F. HOGAN ◽  
NATHALIE ESSER ◽  
ANDREW T. TEMPLIN ◽  
JOSEPH J. CASTILLO ◽  
SAKENEH ZRAIKA ◽  
...  
Keyword(s):  
Protein Expression ◽  
Regulatory Protein ◽  
Steroidogenic Acute Regulatory Protein ◽  
Islet Amyloid ◽  
Chronic Activation ◽  
Steroidogenic Acute Regulatory

scholarly journals An insight on promising strategies hoping to cure HIV-1 infection by targeting Rev protein—short review

2021 ◽  
Author(s):  
Sahana Pai ◽  
Jayesh Mudgal ◽  
B. Venkatesh Kamath ◽  
K. Sreedhara Ranganath Pai
Keyword(s):  
Reverse Transcriptase ◽  
Regulatory Protein ◽  
Short Review ◽  
Fixed Dose ◽  
Reverse Transcriptase Inhibitors ◽  
Nucleoside Reverse Transcriptase Inhibitors ◽  
Promising Therapeutic Target ◽  
Latent Hiv ◽  
Approved Drugs ◽  
Hiv 1

AbstractHuman immunodeficiency virus-1 (HIV-1) infection remains to be one of the major threats throughout the world. Many researchers are working in this area to find a cure for HIV-1. The group of the FDA approved drugs which are currently used against HIV-1 in the clinical practice include nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), integrase inhibitors (InIs), and protease inhibitors (PIs). Fixed dose combinations (FDCs) of these drugs are available and are used as per the anti-retroviral therapy (ART) guidelines. Despite these, unfortunately, there is no cure for HIV1 infection to date. The present review is focused upon describing the importance of a post-transcriptional regulatory protein “Rev”, responsible for latent HIV-1 infection as a possible, and promising therapeutic target against HIV-1.

HIV-1 tat protein expression in mouse brain potentiates ethanol reward and reinstates extinguished ethanol-seeking behavior

2014 ◽  
Vol 140 ◽  
pp. e141-e142
Author(s):  
Jay P. McLaughlin ◽  
M.L. Ganno ◽  
S.O. Eans ◽  
Jason J. Paris ◽  
H.D. Singh
Keyword(s):  
Protein Expression ◽  
Mouse Brain ◽  
Tat Protein ◽  
Seeking Behavior ◽  
Hiv 1

scholarly journals Foamy Viruses, Bet, and APOBEC3 Restriction

Viruses ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 504
Author(s):  
Ananda Ayyappan Jaguva Vasudevan ◽  
Daniel Becker ◽  
Tom Luedde ◽  
Holger Gohlke ◽  
Carsten Münk
Keyword(s):  
Current Knowledge ◽  
Regulatory Protein ◽  
Host Population ◽  
Life Cycles ◽  
Restriction Factors ◽  
Host Restriction ◽  
Open Questions ◽  
Foamy Viruses ◽  
Natural Hosts ◽  
Hiv 1

Non-human primates (NHP) are an important source of viruses that can spillover to humans and, after adaptation, spread through the host population. Whereas HIV-1 and HTLV-1 emerged as retroviral pathogens in humans, a unique class of retroviruses called foamy viruses (FV) with zoonotic potential are occasionally detected in bushmeat hunters or zookeepers. Various FVs are endemic in numerous mammalian natural hosts, such as primates, felines, bovines, and equines, and other animals, but not in humans. They are apathogenic, and significant differences exist between the viral life cycles of FV and other retroviruses. Importantly, FVs replicate in the presence of many well-defined retroviral restriction factors such as TRIM5α, BST2 (Tetherin), MX2, and APOBEC3 (A3). While the interaction of A3s with HIV-1 is well studied, the escape mechanisms of FVs from restriction by A3 is much less explored. Here we review the current knowledge of FV biology, host restriction factors, and FV–host interactions with an emphasis on the consequences of FV regulatory protein Bet binding to A3s and outline crucial open questions for future studies.

scholarly journals Double-Stranded RNA Adenosine Deaminases Enhance Expression of Human Immunodeficiency Virus Type 1 Proteins

2008 ◽  
Vol 82 (21) ◽  
pp. 10864-10872 ◽  
Author(s):  
Angsana Phuphuakrat ◽  
Romchat Kraiwong ◽  
Chompunuch Boonarkart ◽  
Darat Lauhakirti ◽  
Tun-Hou Lee ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Protein Expression ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Structural Protein ◽  
Double Stranded Rna ◽  
Adenosine Deaminases ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT ADARs (adenosine deaminases that act on double-stranded RNA) are RNA editing enzymes that catalyze a change from adenosine to inosine, which is then recognized as guanosine by translational machinery. We demonstrate here that overexpression of ADARs but not of an ADAR mutant lacking editing activity could upregulate human immunodeficiency virus type 1 (HIV-1) structural protein expression and viral production. Knockdown of ADAR1 by RNA silencing inhibited HIV-1 production. Viral RNA harvested from transfected ADAR1-knocked-down cells showed a decrease in the level of unspliced RNA transcripts. Overexpression of ADAR1 induced editing at a specific site in the env gene, and a mutant with the edited sequence was expressed more efficiently than the wild-type viral genome. These data suggested the role of ADAR in modulation of HIV-1 replication. Our data demonstrate a novel mechanism in which HIV-1 employs host RNA modification machinery for posttranscriptional regulation of viral protein expression.

Cocaine-seeking is dose dependently enhanced by HIV-1 tat protein expression in male and female mice

2014 ◽  
Vol 140 ◽  
pp. e168
Author(s):  
Jason J. Paris ◽  
A.N. Carey ◽  
Jay P. McLaughlin
Keyword(s):  
Protein Expression ◽  
Tat Protein ◽  
Male And Female ◽  
Female Mice ◽  
Cocaine Seeking ◽  
Hiv 1

scholarly journals HIV-1 auxiliary regulatory protein Vpr promotes ubiquitination and turnover of Vpr mutants containing the L64P mutation

FEBS Letters ◽  
2004 ◽  
Vol 563 (1-3) ◽  
pp. 170-178 ◽  
Author(s):  
Ling-Jun Zhao ◽  
Heng Jian ◽  
Henghu Zhu
Keyword(s):  
Regulatory Protein ◽  
Hiv 1

scholarly journals Enhanced expression of the complement regulatory protein, membrane inhibitor of reactive lysis (CD59), is regulated at the level of transcription

Blood ◽  
1993 ◽  
Vol 82 (3) ◽  
pp. 968-977
Author(s):  
MH Holguin ◽  
CB Martin ◽  
JH Weis ◽  
CJ Parker
Keyword(s):  
Protein Expression ◽  
Blot Analysis ◽  
Interleukin 1 ◽  
Critical Role ◽  
Regulatory Protein ◽  
Calcium Ionophore ◽  
Cytolytic Activity ◽  
Host Cells ◽  
Rna Expression ◽  
Enhanced Expression

The membrane inhibitor of reactive lysis (MIRL) is an 18-Kd glycosyl phosphatidylinositol anchored membrane glycoprotein that inhibits the cytolytic activity of complement. MIRL is expressed by all hematopoietic elements and by a wide variety of nonhematopoietic tissues. A deficiency of MIRL is primarily responsible for the greater sensitivity of the erythrocytes of paroxysmal nocturnal hemoglobinuria to complement mediated lysis. Because of its critical role in protecting host cells from injury by complement, we hypothesized that mechanisms exist that allow MIRL expression to be regulated. To investigate this hypothesis, both MIRL RNA and MIRL protein expression were analyzed following exposure of K562 erythroleukemia cells to a variety of potential stimulants. Incubation with dexamethasone, calcium ionophore, lipopolysaccharide, interleukin 1, tumor necrosis factor, hemin, and cyclic AMP had no effect on MIRL expression. However, incubation with phorbol 12-myristate 13 acetate (PMA), induced a marked increase in MIRL RNA as determined by Northern blot analysis. This enhanced expression of MIRL RNA was associated with an increase in MIRL protein expression as determined by immunoprecipitation of metabolically labeled proteins, Western blot analysis, and immunobinding assay. Enhanced MIRL RNA expression was first detected after 8 hours and increased through 24 hours of observation. Inhibitors of either protein synthesis or transcription abrogated the PMA-induced enhancement of MIRL RNA expression. Together, these results are consistent with a model in which PMA induces synthesis of a trans acting protein that enhances transcription of the MIRL gene.

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